Post by Nancy Stagliano

The past few weeks have sparked important conversations across the Parkinson’s disease community. As our industry continues to evaluate recent results in Parkinson’s drug development, one thing remains clear to me: Parkinson’s disease is not a single disease, and meaningful progress will require us to better understand the biology driving disease in individual patients. The urgency I feel around this work is deeply personal. I began my career as an engineer before following my curiosity into neuroscience and ultimately drug development. Along the way, I experienced firsthand the devastating impact that serious diseases can have on families. Losing my father to Progressive Supranuclear Palsy (PSP), a rare neurodegenerative disease, while I was completing my Ph.D., and later losing my mother and uncle to pancreatic cancer, reinforced a lesson that I carry with me every day: patients can’t wait for incremental progress. Those experiences also taught me that meaningful progress often comes from embracing complexity rather than avoiding it. The most important problems in medicine are rarely solved in a straight line. Scientific progress is built through persistence, learning and a willingness to challenge conventional thinking. Every study teaches us something, and every lesson brings us closer to helping those individuals who are still waiting. Breakthroughs don’t happen overnight, nor are they the result of a single experiment. For decades, Parkinson’s disease drug development has largely taken an “all-comers” approach, treating Parkinson’s as though it were a single disease. Yet researchers increasingly recognize that different people likely arrive at Parkinson’s through different biological pathways. If this is true, then it stands to reason that the most effective therapies will be designed for the individuals whose disease is driven by a specific underlying mechanism. That conviction is what brought me to Neuron23, and it remains the foundation of our work today. We are pursuing a precision medicine approach to Parkinson’s disease by identifying people whose disease is driven by overactive LRRK2 biology and evaluating whether targeted inhibition of that pathway can slow disease progression. Rather than assuming a therapy works for everyone, we invested a considerable amount of research into understanding who is most likely to benefit and why. The future of Parkinson’s treatment will not be built on a one-size-fits-all approach. I believe it will be built on a deeper understanding of disease biology and a commitment to bringing the right therapies to the right patients. We still have much to learn, but I believe we are asking better questions than ever before. BioCentury article link: https://lnkd.in/gEpAsuDQ